Structure and strength in causal induction

We present a framework for the rational analysis of elemental causal induction-learning about the existence of a relationship between a single cause and effect-based upon causal graphical models. This framework makes precise the distinction between causal structure and causal strength: the difference between asking whether a causal relationship exists and asking how strong that causal relationship might be. We show that two leading rational models of elemental causal induction, DeltaP and causal power, both estimate causal strength, and we introduce a new rational model, causal support, that assesses causal structure. Causal support predicts several key phenomena of causal induction that cannot be accounted for by other rational models, which we explore through a series of experiments. These phenomena include the complex interaction between DeltaP and the base-rate probability of the effect in the absence of the cause, sample size effects, inferences from incomplete contingency tables, and causal learning from rates. Causal support also provides a better account of a number of existing datasets than either DeltaP or causal power.     

Time and Singular Causation—A Computational Model

Causal queries about singular cases, which inquire whether specific events were causally connected, are prevalent in daily life and important in professional disciplines such as the law, medicine, or engineering. Because causal links cannot be directly observed, singular causation judgments require an assessment of whether a co-occurrence of two events c and e was causal or simply coincidental. How can this decision be made? Building on previous work by Cheng and Novick (2005) and Stephan and Waldmann (2018), we propose a computational model that combines information about the causal strengths of the potential causes with information about their temporal relations to derive answers to singular causation queries. The relative causal strengths of the potential cause factors are relevant because weak causes are more likely to fail to generate effects than strong causes. But even a strong cause factor does not necessarily need to be causal in a singular case because it could have been preempted by an alternative cause. We here show how information about causal strength and about two different temporal parameters, the potential causes' onset times and their causal latencies, can be formalized and integrated into a computational account of singular causation. Four experiments are presented in which we tested the validity of the model. The results showed that people integrate the different types of information as predicted by the new model.     

Learning the form of causal relationships using hierarchical bayesian models

People learn quickly when reasoning about causal relationships, making inferences from limited data and avoiding spurious inferences. Efficient learning depends on abstract knowledge, which is often domain or context specific, and much of it must be learned. While such knowledge effects are well documented, little is known about exactly how we acquire knowledge that constrains learning. This work focuses on knowledge of the functional form of causal relationships; there are many kinds of relationships that can apply between causes and their effects, and knowledge of the form such a relationship takes is important in order to quickly identify the real causes of an observed effect. We developed a hierarchical Bayesian model of the acquisition of knowledge of the functional form of causal relationships and tested it in five experimental studies, considering disjunctive and conjunctive relationships, failure rates, and cross-domain effects. The Bayesian model accurately predicted human judgments and outperformed several alternative models.     

Diagnostic causal reasoning with verbal information

In diagnostic causal reasoning, the goal is to infer the probability of causes from one or multiple observed effects. Typically, studies investigating such tasks provide subjects with precise quantitative information regarding the strength of the relations between causes and effects or sample data from which the relevant quantities can be learned. By contrast, we sought to examine people’s inferences when causal information is communicated through qualitative, rather vague verbal expressions (e.g., “X occasionally causes A”). We conducted three experiments using a sequential diagnostic inference task, where multiple pieces of evidence were obtained one after the other. Quantitative predictions of different probabilistic models were derived using the numerical equivalents of the verbal terms, taken from an unrelated study with different subjects. We present a novel Bayesian model that allows for incorporating the temporal weighting of information in sequential diagnostic reasoning, which can be used to model both primacy and recency effects. On the basis of 19,848 judgments from 292 subjects, we found a remarkably close correspondence between the diagnostic inferences made by subjects who received only verbal information and those of a matched control group to whom information was presented numerically. Whether information was conveyed through verbal terms or numerical estimates, diagnostic judgments closely resembled the posterior probabilities entailed by the causes’ prior probabilities and the effects’ likelihoods. We observed interindividual differences regarding the temporal weighting of evidence in sequential diagnostic reasoning. Our work provides pathways for investigating judgment and decision making with verbal information within a computational modeling framework.     

From mere coincidences to meaningful discoveries

People's reactions to coincidences are often cited as an illustration of the irrationality of human reasoning about chance. We argue that coincidences may be better understood in terms of rational statistical inference, based on their functional role in processes of causal discovery and theory revision. We present a formal definition of coincidences in the context of a Bayesian framework for causal induction: a coincidence is an event that provides support for an alternative to a currently favored causal theory, but not necessarily enough support to accept that alternative in light of its low prior probability. We test the qualitative and quantitative predictions of this account through a series of experiments that examine the transition from coincidence to evidence, the correspondence between the strength of coincidences and the statistical support for causal structure, and the relationship between causes and coincidences. Our results indicate that people can accurately assess the strength of coincidences, suggesting that irrational conclusions drawn from coincidences are the consequence of overestimation of the plausibility of novel causal forces. We discuss the implications of our account for understanding the role of coincidences in theory change.     

The evolution of frequency distributions: Relating regularization to inductive biases through iterated learning

The regularization of linguistic structures by learners has played a key role in arguments for strong innate constraints on language acquisition, and has important implications for language evolution. However, relating the inductive biases of learners to regularization behavior in laboratory tasks can be challenging without a formal model. In this paper we explore how regular linguistic structures can emerge from language evolution by iterated learning, in which one person’s linguistic output is used to generate the linguistic input provided to the next person. We use a model of iterated learning with Bayesian agents to show that this process can result in regularization when learners have the appropriate inductive biases. We then present three experiments demonstrating that simulating the process of language evolution in the laboratory can reveal biases towards regularization that might not otherwise be obvious, allowing weak biases to have strong effects. The results of these experiments suggest that people tend to regularize inconsistent word-meaning mappings, and that even a weak bias towards regularization can allow regular languages to be produced via language evolution by iterated learning.     

Do We “do”?

A normative framework for modeling causal and counterfactual reasoning has been proposed by Spirtes, Glymour, and Scheines (1993; cf. Pearl, 2000). The framework takes as fundamental that reasoning from observation and intervention differ. Intervention includes actual manipulation as well as counterfactual manipulation of a model via thought. To represent intervention, Pearl employed the do operator that simplifies the structure of a causal model by disconnecting an intervened-on variable from its normal causes. Construing the do operator as a psychological function affords predictions about how people reason when asked counterfactual questions about causal relations that we refer to as undoing, a family of effects that derive from the claim that intervened-on variables become independent of their normal causes. Six studies support the prediction for causal (A causes B) arguments but not consistently for parallel conditional (if A then B) ones. Two of the studies show that effects are treated as diagnostic when their values are observed but nondiagnostic when they are intervened on. These results cannot be explained by theories that do not distinguish interventions from other sorts of events.     

Causal judgements about two causal candidates: Accounting for occurrences,estimating strength,and the importance of interaction judgements

When two possible causes of an outcome are under consideration, contingency information concerns each possible combination of presence and absence of the two causes with occurrences and nonoccurrences of the outcome. White (2008) proposed that such judgements could be predicted by a weighted averaging model integrating these kinds of contingency information. The weights in the model are derived from the hypothesis that causal judgements seek to meet two main aims, accounting for occurrences of the outcome and estimating the strengths of the causes. Here it is shown that the model can explain many but not all relevant published findings. The remainder can be explained by reasoning about interactions between the two causes, by scenario-specific effects, and by variations in cell weight depending on quantity of available information. An experiment is reported that supports this argument. The review and experimental results support the case for a cognitive model of causal judgement in which different kinds of contingency information are utilised to satisfy particular aims of the judgement process.